To fuse, membranes must bend. The energy of the unknown bent intermediates of biological fusion in diverse physiological processes depends on the ability of membrane lipids support the required curvatures. We have studied the effects of membrane lipid composition on the rates of fusion reaction. Lipids of the different molecular shapes such as inverted cone-shaped lysophosphatidylcholine, LPC, and cone- shaped arachidonic acid, AA, were added exogenously to membranes to alter their propensity to bend. Addition of LPC to contacting monolayers of cell membranes inhibited low pH triggered cell-cell fusion mediated by the specialized envelope proteins of baculovirus (gp64) and influenza virus (hemagglutinin). In contrast, AA promoted these fusion reactions. Modulation of membrane lipid composition reversibly affected fusion (inhibited or promoted) at a stage of actual merger of membrane lipid bilayers which follow the triggering of fusion. To elucidate the mechanisms of lipid bilayer fusion in the well defined model system we studied the fusion of phospholipid vesicles to planar phospholipid bilayer membranes. Two distinct fusion stages, hemi- and complete fusion (i.e., membranes' lipid mixing without and with fusion pore formation, respectively) were established. Hemifusion was prevented by adding inverted cone-shaped LPC to contacting monolayers of two fusing membranes. In contrast, fusion pore formation depended on the composition of distal monolayers: LPC promoted and cone-shaped AA inhibited complete fusion. Thus, lipids differentially modulate membrane fusion by stages according to lipid shape and place. The similarity between effects of the membrane lipid composition obtained for fusion of model lipid membranes and those for biological membrane fusion supports the hypothesis that stalk (local connection between two membranes leading to membrane hemifusion) and pore types of fusion intermediates may be involved in the biological fusion.